Cardiac arrest (CA) is a fatal disease with high rates of neurological impairment. At present, targeted temperature management (TTM) is the only strategy with firm clinical evidence to prove its effectiveness. However, there is still controversy on the implementation of TTM, particularly on its depth, with a lack of elucidated underlying therapeutic mechanisms. Six Wistar rats were subjected to 8 min asphyxia-CA and randomly divided into TTM at 33oC(n=3) or 35° C groups (n=3). The spatiotemporal characteristics of cerebral glucose metabolism after CA were investigated by 18F-FDG microPET/CT. Myelin Basic Protein (MBP) immunofluorescence staining was used to assess acute injury and recovery of oligodendrocytes. Functional recovery was evaluated using the neurological deficit score (NDS). There was a significant improvement in functional recovery by NDS (p < 0.05) in the 33oC group compared with the 35° C group. Glucose metabolism of the 33° C group was higher than that of the 35oC group early after resuscitation (within 10 minutes). Immunofluorescence analysis showed that positive MBP signals in the cortex and hippocampus in the 33oC group were greater than in the 35oC group. In conclusion, compared to 35oC TTM, 33° C TTM changed the spatiotemporal characteristics of brain glucose metabolisms with improved neurological function, which may be through oligodendrocyte participation.